According to the influential “pulsed inhibition hypothesis” (Jensen and Mazaheri, FHN 2010), the 8–14Hz alpha oscillation, termed μ-rhythm in the sensorimotor cortex, is driven by bouts of inhibition (or deflections of the cortical excitation-inhibition balance towards inhibition), rhythmically suppressing neural processing during the inhibitory phase, while permitting it during the excitable phase (or “duty cycle”). Since alpha is supposed to be asymmetric (Mazaheri and Jensen, JN 2008; Schalk, FHN 2015), increasing amplitudes would result from stronger bouts of inhibition rather that excitation, thereby gradually shortening the duration of the duty cycle during which local neural processing can occur. Indeed, sensorimotor μ-rhythm power (Sauseng et al., Neuropsychologia 2009) and phase (Zrenner et al., submitted for publication) have been found to modulate corticospinal excitability, as indexed by the amplitude of motor evoked responses (MEPs) elicited by transcranial magnetic stimulation (TMS) of the primary motor cortex (M1). However, the asymmetry of the oscillation and its proposed inhibitory nature have not yet been explicitly tested. Here we set out to explicitly test the “pulsed inhibition hypothesis” by disentangling the contribution of μ-rhythm power and phase to the modulation of both cortical excitability and inhibition, measuring the GABA-A-receptor mediated short intra-cortical inhibition (SICI) via EEG-triggered paired-pulse TMS. SICI consists of a conditioning stimulus (CS) at subthreshold stimulation intensity followed by a test stimulus (TS) at suprathreshold intensity with an inter-stimulus interval (ISI) of 2.0ms. Here, CS+TS and TS alone trials are randomly intermingled and EEG-triggered in real-time based on the online extracted μ-rhythm to target two power levels (high, low) and four different phase angles (rising flank, peak, falling flank, trough). The real-time EEG-triggered TMS setup consists of a NeurOne 64-channel EEG system feeding the signal of all channels into a real-time computer, which is running the analyses via a Simulink model and triggers four monophasic Magstim 2002 systems connected to a single coil via the Magstim 4-into-1 module to allow shorter inter-trial intervals (∼2s) and fully flexible external control. MEP amplitudes are analyzed in an amplitude- and phase-dependent manner to characterize the GABA-A-ergic profile of human sensorimotor μ-rhythm and thereby test a fundamental assumption of the “pulsed inhibition hypothesis”.